Host induces a robust antiviral gene program, when it senses a viral infection that is rapid but transient, quickly entering resolution phase to limit autoimmune pathology. The transient nature is attributed to the instability motifs encoded in the 3'UTR of antiviral genes. These instability motifs can be targeted by RNA-binding proteins, miRNAs, or long non-coding RNAs leading to degradation of mRNA. To limit pathology, host switches from an ?antiviral? to a ?resolution? phase by inducing post-transcriptional regulators to downregulate antiviral genes. While viral inhibition of the host?s pathogen sensing pathways is well described, a viral strategy accelerating the resolution phase post-transcriptionally remains unexplored. We hypothesize that viruses hijack the host post- transcriptional program to block the antiviral immune response and expedite the resolution phase. Specifically, we propose that they decrease the stability of antiviral genes by prematurely inducing RNA binding proteins, non-coding RNAs, or alternative polyadenylation to include more instability motifs. We take an integrative approach to understand the role of post-transcriptional control in defining the host-pathogen interactions by coupling robust computational approaches with functional studies. SA1: Do post-transcriptional regulators resolve antiviral activity? SA2: Does virus induce post-transcriptional regulators to accelerate the resolution phase as an immune evasion strategy? SA3. How does the host counteract viral immune evasion at the post- transcriptional interface? We will gain insights into the role of post-transcriptional gene silencing in the resolution of antiviral inflammation. Interaction of these pathways remain unexplored, potentially providing novel mechanistic insights into viral pathogenesis. This work will define a novel interphase where the host-pathogen could interact potentially providing new therapeutic targets for new and emerging viruses.